ライフサイエンスコーパス: renal injury

1 flammatory response that exacerbate ischemic renal injury.

2 suspected mechanism of vancomycin-associated renal injury.

3 L) has been implicated in the development of renal injury.

4 contributes importantly to the intensity of renal injury.

5 mmation are integral to hypertension-induced renal injury.

6 ase Shp2 to lipopolysaccharide (LPS)-induced renal injury.

7 nsplantation (RTx) and in vitro cold hypoxic renal injury.

8 il dwell time and ROS production, as well as renal injury.

9 )CD25(+) cells were also found as increasing renal injury.

10 del of human salt-sensitive hypertension and renal injury.

11 into the kidney exacerbates hypertension and renal injury.

12 , which might inhibit or potentially reverse renal injury.

13 wild-type mice, with respect to survival and renal injury.

14 , and whether the kidneys were challenged by renal injury.

15 he feasibility of a novel therapy to curtail renal injury.

16 increases the hazard rate of having rash and renal injury.

17 irected to recipient-dependent mechanisms of renal injury.

18 of Rhophilin-1 knockout mice exacerbated the renal injury.

19 tment normalized blood pressure and reversed renal injury.

20 (MV) rarefaction in RVD, a major feature of renal injury.

21 tial as a strategy for improving outcomes of renal injury.

22 nd the progression is further accelerated by renal injury.

23 7A in innate leukocytes in cisplatin-induced renal injury.

24 g crystal morphology, crystal clearance, and renal injury.

25 -17A from those cells does not contribute to renal injury.

26 rted into proximal tubules, leading to acute renal injury.

27 nergy metabolism and attenuating I/R-induced renal injury.

28 markedly increasing their susceptibility to renal injury.

29 conditions and fostering macrophage-mediated renal injury.

30 ed in wild-type mice after cisplatin-induced renal injury.

31 sed albuminuria and histological measures of renal injury.

32 nflammation, thereby attenuating I/R-induced renal injury.

33 ession protected animals from L-NAME-induced renal injury.

34 ich in turn contribute to the progression of renal injury.

35 oteins, can attenuate both acute and chronic renal injury.

36 nhibitors in the setting of acute or chronic renal injury.

37 malities and those with sustained iatrogenic renal injury.

38 rization in ARAS on renal tissue hypoxia and renal injury.

39 rstitial injury, and decreased biomarkers of renal injury.

40 ry response to IRI exacerbates the resultant renal injury.

41 ells (Tregs) help protect against autoimmune renal injury.

42 ause hemolytic anemia, thrombocytopenia, and renal injury.

43 ly demonstrated in the pathogenesis of acute renal injury.

44 diac fibrosis with calcifications, and focal renal injury.

45 development but increased susceptibility to renal injury.

46 TL1A), and TNF in TECs, as observed in human renal injury.

47 is in five mouse models of acute and chronic renal injury.

48 recruitment into the kidney and ameliorated renal injury.

49 a target for novel therapeutic approaches to renal injury.

50 onferred protection against diabetes-induced renal injury.

51 in Ins2(Akita) mice or STZ-induced diabetic renal injury.

52 dies in the broader context of immunological renal injury.

53 um reabsorption, proliferation, fibrosis and renal injury.

54 gesting that it may protect against ischemic renal injury.

55 stabilizes the obstructed kidney and limits renal injury.

56 ported to be markedly induced in response to renal injury.

57 fter renal I/R and contributes to functional renal injury.

58 -, cisplatin-, and rhabdomyolysis-associated renal injury.

59 ional adult cilia mutant mice by introducing renal injury.

60 crystal-induced inflammasome activation and renal injury.

61 mes associated with rhabdomyolysis and acute renal injury.

62 the activation of Th17 cells and influences renal injury.

63 s leading to ELA, a detrimental event toward renal injury.

64 gulated EGFR activation mediates progressive renal injury.

65 up 2 innate lymphoid cells (ILC2) to prevent renal injury.

66 iferative, regression, and chronic phases of renal injury.

67 otected against ischemia-reperfusion-induced renal injury.

68 hropathy and mice with hyperglycemia-induced renal injury.

69 lication in protection from ischemic-induced renal injury.

70 d renal function and reduced the severity of renal injury.

71 cant attenuation of intestinal, hepatic, and renal injuries.

72 sation, which complicates ~30% of high-grade renal injuries.

73 ration was associated with increased risk of renal injury (6.2% vs. 2.9%; absolute risk difference 13

74 Severe renal injuries after blunt trauma cause diagnostic and t

75 ntly and attenuated intestinal, hepatic, and renal injury after AKI.

76 ocardial infarction, bleeding, and recurrent renal injury after discharge.

77 Our results indicate that octreotide reduced renal injury after HIR due to its induction of autophagy

78 However, nonperitoneal B cells attenuate renal injury after I/R, possibly through the production

79 We also assessed hepatic and renal injury after intestinal IRI.

80 th S1P(2)R small interfering RNA had reduced renal injury after IR.

81 ore IRI protects from both acute and chronic renal injuries and may have clinical application in prot

82 ssment of altered redox capacity in diabetic renal injury and after successful treatment.

83 erlipidemia acted reciprocally, accentuating renal injury and altering renal function.

84 nuating systemic inflammation in health, and renal injury and aortic calcification despite hyperphosp

85 ed renal function, and attenuated histologic renal injury and apoptosis after IRI.

86 eceptor agonist exendin-4 reduced CP-induced renal injury and apoptosis, and suppression of renal GLP

87 and multiple organ failure, including acute renal injury and ARDS.

88 monstrated equal efficacy but with decreased renal injury and bone mineral density loss compared with

89 Calcineurin inhibitors cause vascular and renal injury and can trigger hemolytic uremic syndrome.

90 Interestingly, both the renal injury and dysfunction in wild-type mice undergoin

91 ent with the three rhubarb extracts improved renal injury and dysfunction, either fully or partially

92 cisplatin, Tlr9(-/-) mice developed enhanced renal injury and exhibited fewer intrarenal regulatory T

93 brosis, whereas TPH-1 deficiency exacerbates renal injury and fibrosis by activating NF-kappaB and in

94 ther TLR-4 deficiency reduces Ang-II-induced renal injury and fibrosis by attenuating reactive oxygen

95 CL16 plays a key role in the pathogenesis of renal injury and fibrosis in salt-sensitive hypertension

96 ugh angiotensin II (AngII) is known to cause renal injury and fibrosis, the underlying mechanisms rem

97 e TGFbeta signaling pathway to contribute to renal injury and fibrosis.

98 esults strongly support a role for IRAK-M in renal injury and identify IRAK-M as a possible modulator

99 igh) population associated with the onset of renal injury and increase in proinflammatory cytokines,

100 hypertension, microvascular rarefaction, and renal injury and led to greater recovery of renal functi

101 recipients who showed evidence of reversible renal injury and limited chronicity on pre-LT kidney bio

102 and dedifferentiation, which associate with renal injury and may also influence the rate of cystogen

103 role for complement activation in BD-induced renal injury and postulate complement blockade as a prom

104 iptin (AG), significantly reduced CP-induced renal injury and reduced the renal mRNA expression ratio

105 Both renal injury and renal IL-1beta and IL-17A production we

106 We hypothesized that ADC may indicate renal injury and response to therapy in patients with re

107 plays a major role in induction of diabetic renal injury and that blocking arginase-2 activity or ex

108 f the pathogenesis of alcohol-induced hepato-renal injury and the development of new approaches to it

109 e found that induction of HO attenuated both renal injury and the rate of cystogenesis, whereas inhib

110 ic landscape at the single-cell level during renal injury and the resolution of fibrosis.

111 mmation, endothelial damage, thrombosis, and renal injury and underscore ongoing risk for systemic TM

112 ion, acute respiratory failure, and/or acute renal injury), and absolute lymphocyte count less than o

113 maternal and pup weights, lower pup number, renal injury, and a larger heart compared to a control g

114 ays, had increased biochemical indicators of renal injury, and exhibited severe pathological injury w

115 ificantly reduced TRL, as well as markers of renal injury, and improved endothelial-dependent vasorel

116 associated with increased aortic stiffness, renal injury, and incident cardiovascular events.

117 t mortality, worse structural and functional renal injury, and increased levels of apoptosis in rhabd

118 xpression normalized systolic BP, attenuated renal injury, and inhibited RPTC Nrf2, Agt, and heme oxy

119 subsequent HSRs, including documented rash, renal injury, and liver injury.

120 stations (microangiopathy, thrombocytopenia, renal injury, and thrombophilia) of COVID-19 that are al

121 cteria capable of causing pyelonephritis and renal injury, and to selectively target the gastrointest

122 trarenal RAS thereby control blood pressure, renal injury, and urine concentrating ability in health

123 Novel biomarkers of renal injury appear inconsistent in identifying a creati

124 and age, hemoglobin and markers of liver and renal injury are associated with inflammation.

125 yte infiltration, and inflammation following renal injury as determined by light microscopy, immunohi

126 that were produced in a mouse model of acute renal injury (as a result of kidney-specific ablation of

127 irectly to mice with ischemic AKI attenuated renal injury, as assessed by plasma creatinine, tubular

128 ression was measured using real-time PCR and renal injury assessed with histological analysis.

129 sease (DKD), which involves glucose-mediated renal injury associated with a disruption in mitochondri

130 e in the proximal tubule, may be involved in renal injury associated with ageing.

131 ney disease in blacks, but the mechanisms of renal injury associated with APOL1 risk variants are unk

132 tion of Epac as a therapeutic application in renal injury associated with oxidative stress.

133 Soluble apyrase reduced acute renal injury at 24 hours and renal fibrosis at 4 weeks p

134 39 transgenic mice were protected from acute renal injury at 24 hours, but had increased renal fibros

135 ach that will help to define the pathways of renal injury at a cellular level.

136 suggest that the VDR attenuates obstructive renal injury at least in part by suppressing the renin-a

137 alin and varying creatinine-based metrics of renal injury at multiple time points associated with car

138 py attenuated MV damage, but did not resolve renal injury at practical clinical doses.

139 Doses>/=0.1 mg/kg DA elevated the renal injury biomarkers kidney injury molecule-1 and neu

140 measured in air, urine, and serum, and early renal injury biomarkers were measured in urine.

141 t augments Treg and ILC2 to not only inhibit renal injury, but also promote regeneration.

142 human tubular epithelial cells (TECs) during renal injury, but its function in this setting remains u

143 Bone marrow-derived stem cells may modulate renal injury, but the effects may depend on the age of t

144 -214 and miR-21 are upregulated in models of renal injury, but the function of miR-214 in this settin

145 enzyme involved in 5-MTP synthesis, reduces renal injury by attenuating renal inflammation and fibro

146 hat is distinguishable from typical ischemic renal injury by its paucity of tubular cell death.

147 s9 to generate mouse models and assessed for renal injury by measuring albuminuria and examining kidn

148 ies) limits the progression of pulmonary and renal injury by reducing activation of the AGEs-RAGE pat

149 type and eNOS knockout mice and then induced renal injury by uninephrectomy.

150 Renal injury can also markedly accelerate the renal cyst

151 ation either before, late or very late after renal injury can restore kidney structure and function.

152 echanism that may be involved in progressive renal injury caused by chronic exposure to Ang II.

153 l and histological features that may lead to renal injury caused by thrombosis at any location within

154 mportantly, aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly rever

155 Periostin overexpression protected mice from renal injury compared with controls, whereas knockout mi

156 malfunction, tissue failure, and progressive renal injury despite cystine-depletion therapies.

157 However, renal injury did not induce the expression of Bpifa2 in

158 of fibrosis/tissue remodeling, inflammation, renal injury/dysfunction, and liver fibrosis.

159 treptozotocin model of hyperglycemia-induced renal injury ENaC activity in hyperglycemic animals was

160 s in mice fed an adenine diet known to cause renal injury followed by fibrosis.

161 In addition, intestinal, hepatic, and renal injury following AKI was attenuated without affect

162 ficantly attenuated intestinal, hepatic, and renal injury following liver IR.

163 can Association for Surgery of Trauma (AAST) renal injury grading scale.

164 Warfarin-associated calciphylaxis without renal injury has been described, but whether it is a sub

165 MM-associated renal injury has been linked to an excess level of monoc

166 nderstanding of the drivers of MM-associated renal injury has potential for the identification of pro

167 Several biomarkers of renal injury have been identified but the utility of the

168 In mice, GTCs injected after ischemic renal injury homed to the renal parenchyma, and GTC-trea

169 HR], 4.16; 95% CI, 2.54-6.83; P < .0001) and renal injury (HR, 2.13; 95% CI, 1.36-3.33; P = .0009) bu

170 ing to a significant reduction in markers of renal injury, improvement in indicators of renal functio

171 AC6 is a key mediator of cyst formation and renal injury in a model of PKD.

172 about environmental exposure to melamine and renal injury in adults is lacking.

173 ls separated from diseased kidney aggravated renal injury in AN mice.

174 and that FGFR4 does not promote or mitigate renal injury in animal models of CKD.

175 during postnatal renal maturation and after renal injury in control and conditional Ift88 cilia muta

176 butes to the development of hypertension and renal injury in Dahl salt-sensitive (SS) rats, a widely

177 effects of diet supplementation of AS-IV on renal injury in db/db mice, a type 2 diabetic mouse mode

178 Renal injury in diabetes is associated with elevated sys

179 in the kidney plays a key role in mediating renal injury in diabetes.

180 sion and the development of hypertension and renal injury in diabetic Akita transgenic mice.

181 pril also failed to prevent hypertension and renal injury in diabetic eNOSKO mice.

182 on, and attenuates systemic hypertension and renal injury in diabetic Hnrnpf-transgenic (Tg) mice.

183 which hyperglycemia induces hypertension and renal injury in diabetic mice.

184 ike protein (DsbA-L) prevented lipid-induced renal injury in diabetic nephropathy (DN). However, the

185 iated glomerular neutrophil accumulation and renal injury in experimental, crescentic anti-GBM nephri

186 , testosterone increased EGFR expression and renal injury in female Dsk5 mice.

187 for promoting these effects and aggravating renal injury in HIV-transgenic mice.

188 ibution of IgG Fcgamma receptors to diabetic renal injury in hyperglycemic, hypercholesterolemic mice

189 Polygenic susceptibility to renal injury in hypertension arises in association with

190 that contrast strongly in susceptibility to renal injury in hypertension.

191 isplatin-induced functional and histological renal injury in Il17a(-/-) and Rorgammat(-/-) mice, as w

192 nd the factors influencing susceptibility to renal injury in individuals with congenital solitary kid

193 ar events promoting chronic inflammation and renal injury in individuals with DN.

194 of the N- and L-type calcium channel lessens renal injury in kidney disease patients.

195 mulation of VEGFR2 can potentiate subsequent renal injury in mice, an effect enhanced in the setting

196 ibitor trametinib prevents endotoxin-induced renal injury in mice.

197 avel a novel mechanism by which FLCs mediate renal injury in MM by inducing fibrotic and inflammatory

198 podocytes, contributes to the progression of renal injury in mouse GN, and myeloid deficiency of MR p

199 -sepsis model, without observed hemolysis or renal injury in murine toxicity studies.

200 d injury to Fanconi syndrome and progressive renal injury in nephropathic cystinosis.

201 omotes renal ELA and fibrogenesis leading to renal injury in obesity.

202 is a stress-responsive kinase that promotes renal injury in part through phosphorylation-dependent s

203 om April 2013 through June 2014, 13 cases of renal injury in patients receiving dabrafenib therapy we

204 ns and bile acids, might mediate parenchymal renal injury in patients with cirrhosis, suggesting that

205 iated with myocardial injury, mortality, and renal injury in postoperative critical care patients.

206 Furthermore, renal injury in preeclampsia associated with an elevated

207 Cisplatin induced more renal injury in PT-S1P1-null mice than in controls.

208 at treating with aluminum citrate attenuates renal injury in rats with severe ethylene glycol toxicit

209 nd Mas expression, associated with increased renal injury in response to Ang II.

210 1,25-vitamin D3 deficiency directly leads to renal injury in rodents.

211 Lower ADC potentially reflects renal injury in RVD patients, but does not change in res

212 modulate the susceptibility to hypertensive renal injury in SHR-A3 rats.

213 iron accumulation occurs and contributes to renal injury in SLE.

214 butes to the development of hypertension and renal injury in SS rats.

215 te its effects on diabetic macrovascular and renal injury in streptozotocin-induced diabetic apolipop

216 histologic data indicated similar degrees of renal injury in survivin(ptKO) and control mice 24 hours

217 ndothelial nitric oxide synthase accelerates renal injury in the aging kidney.

218 al role of the C5a/C5aR1 axis in propagating renal injury in the development of DKD by disrupting mit

219 llele is defective and likely contributes to renal injury in the FHH rat.

220 To evaluate the effect of IRAK-M in chronic renal injury in vivo, a mouse model of unilateral ureter

221 induced acute tubular necrosis worsened peak renal injury in vivo.

222 We used cisplatin to induce renal injury in wild-type (DR3(+/+)) or congenitally def

223 wed decreased levels of plasma biomarkers of renal injury including Cystatin C, Osteopontin, Tissue I

224 nges that correlate with the three phases of renal injury, including changes in levels of receptors f

225 Antiretroviral drugs also cause renal injury, including crystals and tubular injury, acu

226 with subsequent renal lipid accumulation and renal injury, including glomerulosclerosis, interstitial

227 eatinine and CP caused remarkable pathologic renal injury, including tubular necrosis.

228 6 months after Pkd1 deletion, and additional renal injury increased the likelihood of cyst formation

229 with COPD and/or CS-exposed mice had chronic renal injury, increased urinary albumin/creatinine ratio

230 hat miR-214 functions to promote fibrosis in renal injury independent of TGF-beta signaling in vivo a

231 nary biomarkers in rats during recovery from renal injury induced by exposure to carbapenem A or gent

232 deletion of the MR gene in SMCs, limited the renal injury induced by IR through effects on Rac1-media

233 Renal injury induced by ischemia was associated with inc

234 In mice, renal injury-induced activation of pericytes, which are

235 Renal injury induces the reaccumulation of juvenile-like

236 cteria make targeted probiotic prevention of renal injury-inducing UTIs a potential therapeutic reali

237 Nur77-mediated renal injury involved a conformational change of Bcl2 an

238 Ischemic renal injury is a complex syndrome; multiple cellular ab

239 This attenuated renal injury is associated with reduced oxidative stress

240 of immunological mechanisms in hypertensive renal injury is incompletely understood.

241 urrence of lupus nephritis (LN) before overt renal injury is needed to optimize and individualize tre

242 ciated HUS, and the mechanism of Stx-induced renal injury is not well understood primarily due to a l

243 ion, but the role of integrin alpha2beta1 in renal injury is unclear.

244 During renal injury, kidney-localized proteinases can signal by

245 ssment of polytrauma patients with suspected renal injury, leading to timely diagnosis and urgent sur

246 n together, these data suggest that ischemic renal injury leads to a rise in antibody production, whi

247 layed increased cell death and expression of renal injury marker.

248 l complement activation (C5a and sC5b-9) and renal injury markers (clusterin, cystatin-C, beta2-micro

249 Villin 1 levels were compared with other renal injury markers (creatinine, aspartate transaminase

250 -1alpha, resulted in increased expression of renal injury markers and inflammatory cell infiltration

251 tin-induced nephrotoxicity by reducing these renal injury markers by 40-80% along with a 50-70% reduc

252 nied by elevated levels of muscle, liver and renal injury markers.

253 The increased susceptibility to renal injury may be due, in part, to reduced nephron num

254 Addition of biomarkers of renal injury may provide additional prognostic value to

255 Here, using doxorubicin-induced nephrotoxic renal injury model, we investigated whether IL233 admini

256 rotic cytokine expression in two independent renal injury models: folate nephropathy and unilateral u

257 Hypotension thresholds that provoke renal injury, myocardial injury, and mortality in critic

258 with eosinophilia, including rash (n = 32), renal injury (n = 31), and liver injury (n = 13).

259 ypokalemia, three reported CTC grade 3 acute renal injury, none of which were deemed directly attribu

260 velopment of target organ injury, especially renal injury, obesity-associated hypertension becomes mo

261 In the HES and saline groups, renal injury occurred in 34.6% and 38.0% of patients, re

262 Prolonged obesity and progressive renal injury often lead to the development of treatment-

263 ons with special emphasis on the 5 grades of renal injury on a CT according to the AAST scale.

264 failure conditions influencing or leading to renal injury or dysfunction.

265 talization (OR, 2.9; 95% CI, 1.3-6.7), acute renal injury (OR, 2.7; 95% CI, 1.3-5.6), and CRP on admi

266 ory support, cardiac arrest, hepatic injury, renal injury, or rising lactate level (>5 mmol/l).

267 In VDR knockout mice with renal injury, paricalcitol prevented TRAF3 downregulatio

268 tion of autoantibody production, reversal of renal injury, preservation of biochemical renal function

269 erum creatinine is not a direct indicator of renal injury, rather a surrogate of glomerular function.

270 create a therapeutic target in hypertensive renal injury, rats of both lines were treated with the i

271 d hepatocyte death, cerebral infarction, and renal injury relative to wild-type.

272 dney disease (CKD), but how obesity promotes renal injury remains poorly understood.

273 However, its role in hypertension induced renal injury remains unexplored.

274 eated with the FXR agonist obeticholic acid, renal injury, renal lipid accumulation, apoptosis, and c

275 Notably, after renal injury, renal tubule-forming cells and vessel-form

276 on of the EMT program in TECs during chronic renal injury represents a potential anti-fibrosis therap

277 is a thrombotic microangiopathy with severe renal injury secondary to an overactive alternative comp

278 dministration of a monoclonal antibody after renal injury stimulated bone formation rates, corrected

279 venile than adult kidneys and increase after renal injury, suggesting that cell proliferation may enh

280 enal I/R and found that they sustained worse renal injury than wild-type controls.

281 ity that kidney DDAH1 expression exacerbates renal injury through uromodulin-related mechanisms.

282 lateral urinary obstruction model of chronic renal injury to decipher the role of these enzymes using

283 es the CKD-MBD in diabetic mice subjected to renal injury to induce stage 2 CKD (CKD-2 mice).

284 gleaned from the temporal change markers of renal injury (urine neutrophil gelatinase-associated lip

285 that darunavir protects against HIV-induced renal injury via mechanisms that are independent of inhi

286 H2 S treatment mitigates cold IRI-associated renal injury via mitochondrial actions and could represe

287 e control of salt-sensitive hypertension and renal injury via Rac1, which is one of the small GTPases

288 Acute tubular and glomerular renal injury was accompanied by nonheme iron deposition

289 Renal injury was more common in men (85 men vs 47 women;

290 vestigate the sex differences in response to renal injury, we examined EGFR expression in mice, in hu

291 n this haplotype block and susceptibility to renal injury, we examined the effect of SHR-A3 and SHR-B

292 uld alter susceptibility to hypertension and renal injury, we infused mice with angiotensin II contin

293 To assess renal injury, we performed the renal pelvis injections o

294 ignal transduction pathways mis-regulated in renal injury, we studied the modulation of mammalian tar

295 Serum markers of renal injury were significantly decreased in the CD47mAb

296 tendant complications of multiple myeloma is renal injury, which contributes significantly to morbidi

297 dney/glomerular hypertrophy, and progressive renal injury, which culminates in reduced renal function

298 tension and renal hyperfiltration as well as renal injury with heightened TGF-beta1 expression in adu

299 Mice receiving Adriamycin developed renal injury with loss of podocytes and hyperplastic les

300 onstrates improved hemodynamic responses and renal injury without fetal toxicity following apelin adm